Matthias Dewenter

This study shows that selective class IIa HDAC inhibition improves diastolic dysfunction in HFpEF without adverse effects.

This study shows that reverse cardiac remodeling is a constrained multicellular state with partial recovery of metabolic programs but persistent inflammatory-mitochondrial dysfunction, mediated by lymphatic-derived Reelin.

The paper shows that genomic G quadruplexes regulate mRNA splicing by recruiting RNA-binding proteins, with implications for cardiac function.

The paper identifies CAMK2-NR4A1 signaling as a driver of metabolic substrate switching in heart failure with reduced ejection fraction, linking it to cardiac dysfunction through glucose utilization and lipid depletion.

This study identifies CAMK2D overactivation as the cause of heart failure in RBM20 cardiomyopathy and shows pharmacological inhibition can reverse cardiac dysfunction.

The paper presents TACOMA, a web tool integrating transcriptomics and proteomics data from a TAC-induced heart failure model, revealing molecular mechanisms of cardiac remodelling and failure.